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About:
COVID-19 patients upregulate toll-like receptor 4-mediated inflammatory signaling that mimics bacterial sepsis
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An Entity of Type :
schema:ScholarlyArticle
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covidontheweb.inria.fr
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Type:
Academic Article
research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
COVID-19 patients upregulate toll-like receptor 4-mediated inflammatory signaling that mimics bacterial sepsis
Creator
Kim, Yeon-Sook
Jo, Eun-Kyeong
Cheon, Shinhyea
Kim, Young
Sohn, Kyung
Kim, Hyeon
Kim, In
Jeong, Hyeongseok
Lee, Jooyeon
Lee, Sung-Gwon
Park, Chungoo
Silwal, Prashanta
Source
BioRxiv
abstract
Observational studies of the ongoing coronavirus disease 2019 (COVID-19) outbreak suggest that a cytokine storm is involved in the pathogenesis of severe illness. However, the molecular mechanisms underlying the altered pathological inflammation in COVID-19 are largely unknown. We report here that toll-like receptor (TLR) 4-mediated inflammatory signaling molecules are upregulated in peripheral blood mononuclear cells (PBMCs) from COVID-19 patients, compared with healthy controls. Among the most highly increased inflammatory mediators in severe/critically ill patients, S100A9, an alarmin and TLR4 ligand, was found as a noteworthy biomarker, because it inversely correlated with the serum albumin levels. These data support a link between TLR4 signaling and pathological inflammation during COVID-19 and contribute to develop therapeutic approaches through targeting TLR4-mediated inflammation.
has issue date
2020-07-17
(
xsd:dateTime
)
bibo:doi
10.1101/2020.07.17.207878
has license
biorxiv
sha1sum (hex)
ffbddfa5ea17d89045392354611cac8905bc1194
schema:url
https://doi.org/10.1101/2020.07.17.207878
resource representing a document's title
COVID-19 patients upregulate toll-like receptor 4-mediated inflammatory signaling that mimics bacterial sepsis
schema:publication
bioRxiv
resource representing a document's body
covid:ffbddfa5ea17d89045392354611cac8905bc1194#body_text
is
schema:about
of
named entity 'molecular mechanisms'
named entity 'cytokine storm'
named entity 'mediated'
named entity 'MECHANISMS'
named entity 'UNDERLYING'
named entity 'ILLNESS'
named entity 'illness'
named entity 'CC chemokine ligand'
named entity '5.1'
named entity 'pathogen'
named entity 'NF-κB'
named entity 'TLR4'
named entity 'upregulate'
named entity 'patients'
named entity 'inflammation'
named entity 'coronavirus disease 2019'
named entity 'severe illness'
named entity 'COVID-19'
named entity 'COVID'
named entity 'bacterial sepsis'
named entity 'chest x-ray'
named entity 'molecular mechanisms'
named entity 'chemokine receptor'
named entity 'COVID'
named entity 'antibodies'
named entity 'immune responses'
named entity 'S100A8'
named entity 'Chungnam National University'
named entity 'Immunology'
named entity 'nuclear factor'
named entity 'inflammatory responses'
named entity 'COVID-19 infection'
named entity 'natural killer cell'
named entity 'sputum'
named entity 'interleukin'
named entity 'COVID-19'
named entity 'pathogenesis'
named entity 'KLRB1'
named entity 'differentially expressed'
named entity 'sequelae'
named entity '5.7'
named entity 'Differentially expressed'
named entity 'PBMCs'
named entity 'coronavirus'
named entity 'IRAK1'
named entity 'chemokine'
named entity 'transcriptomic'
named entity 'PBMCs'
named entity 'glucocorticoid receptor'
named entity 'bacterial sepsis'
named entity 'lymphopenia'
named entity 'COVID-19'
named entity 'inflammation'
named entity 'Analyse-it'
named entity 'gene expression'
named entity 'inflammation'
named entity 'chronic kidney disease'
named entity 'lymphocyte'
named entity 'LEF1'
named entity 'interferon regulatory factor'
named entity 'NF-κB'
named entity 'CD14'
named entity 'TLR7'
named entity 'coronavirus disease 2019'
named entity 'pathophysiological'
named entity 'autoimmune diseases'
named entity 'asymptomatic patients'
named entity 'innate immune defense'
named entity 'differentially expressed'
named entity 'TLR8'
named entity 'CCL3'
named entity 'TLR4'
named entity 'TLR7'
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